Paratuberculosis And Crohn's Disease: Got Milk?

by Michael Greger, MD
Updated January 2001

Project Censored

Microbial foodborne illness is the largest class of emerging
infectious diseases. In 1999, the Centers for Disease Control (CDC)
released the latest figures on the incidence of US foodborne illness
considered by the Food and Drug Administration (FDA) to be the most
complete estimate ever compiled. Seventy-six million Americans every
year get food poisoning, more than double the previous estimate. In
today's food safety lottery there's a 1 in 4 chance you'll get sick,
1 in 840 chance you'll be hospitalized and 1 in 55,000 chance that an
American will die from foodborne illness annually.[1]

The CDC estimates 97% of foodborne illness is caused by animal foods.[2] The latest US Department of
Agriculture (USDA) survey, for example, found 9 out of 10
Thanksgiving turkeys--over 90%--are contaminated with campylobacter,
the most common cause of bacterial food poisoning in the US.[3] And 75% of the turkeys are
contaminated with two or more food-borne diseases, most often
salmonella as well, which are becoming dangerously resistant to many
of our best antibiotics.[4]

Although thousands die from food poisoning every year in the
United States, most sufferers only experience acute self-limited
episodes. Up to 15% of those that contract salmonella, however, go on
to get serious joint inflammation that can last for years. An
estimated 100,000 to 200,000 people suffer from arthritis arising
directly from foodborne infections each year it the USA.
NAME="fnB5" HREF="#fn5"[5]

The most feared complication of food poisoning, however, is
Guillain-Barre syndrome, in which infection with campylobacter can
lead to one being paralyzed for months on a ventilator. Up to 3800
cases of Guillain-Barre are triggered by infection with campylobacter
every year in the US. NAME="fnB6" HREF="#fn6"[6]

Some scientists now fear, though, that an even more serious
disease may be contaminating our food supply. Often touted as the
Pulitzer Prize of alternative journalism, a Project Censored Award
was given to what was considered one of the most censored stories of
1999--the connection between Crohn's Disease and paratuberculosis
bacteria in milk.[7]

Crohn's Disease

Described as a human scourge,[8] over a half million[9] Americans suffer from this devastating, lifelong
condition[10] with annual US medical
costs in the billions.[11] Crohn's
sufferers experience profuse urgent diarrhea, nausea, vomiting, and
fevers.[12] Because of the diarrhea,
many people are unable to leave their houses; others drive around in
recreational vehicles or mobile homes to keep a bathroom close at
hand.[13] The director of the
National Association for Colitis and Crohn's Disease says the best
way to describe the disease to non-sufferers if to have them think of
the worst stomach flu they ever had and then try to imagine living
with that every day.[14]

What happens is that the immune system starts attacking the
lining of the gut, which becomes swollen and inflamed.[15] In extreme cases this painful embarrassing
condition can affect any part of the digestive system from the mouth
to the anus.[16] This inflammation
narrows the digestive tract and can result in excruciating pain
during digestion as well as constant uncontrollable bowel movements.
Added discomforts associated with Crohn's disease include severe
joint pains, weight loss and lack of energy.[17]

The intestines characteristically become so deeply ulcerated
that they take on a "cobblestone" appearance. The ulcers can actually
eat right through the gut wall and cause bleeding, abscesses,
fistulas and perforation.[18]
Passing food, sometimes even just drink, through Crohn's damaged
intestines can be excruciatingly painful. In the words of one
colon-rectal surgeon, "Crohn's is a surgical disease. We wait until
the patient can no longer withstand the pain anymore, and then we
perform surgeryŠand repeated surgeries over timeŠultimately, as
recurrences happen and intestinal damage occurs, we just cut and cut,
in some cases, until there is no more intestine that can be cut
out."[19]

Tragically, Crohn's disease typically strikes people in their
teens and early twenties--destroying their health.[20] Children, adolescents, and young adults
suddenly become faced with the harsh reality of a lifetime of chronic
pain, in and out of hospitals their entire lives.[21]

The disease is mostly found in the US, UK and Scandinavia.[22] And it's on the increase. The
incidence in the US, which has been increasing steadily since the
1940's--doubling, then tripling, then quadrupling[23]--is now approaching that of an epidemic.[24] The most rapid increase has been
seen in children. In the 1940's and early 1950's there were no
recorded cases of Crohn's in teenagers. Currently one in every six
new cases diagnosed are under age twenty.[25] Dr. Crohn, who described one of the first
series of cases back in 1932,[26]
wrote decades later "From this small beginning, we have witnessed the
evolution of a Frankenstein monster..."[27]

Johne's Disease

Crohn actually didn't discover Crohn's disease. The first
person to give it a clear description was a Scottish surgeon named
Kennedy Dalziel in 1913.[28] He
wrote "I can only regret that the etiology [cause] of the condition
remains in obscurity, but I trust that before long, further
consideration will clear up the difficulty."[29] Eighty-eight years later and the scientific
community is still not sure what causes Crohn's, but Dalziel had a
hunch which a growing number of prominent scientists now think may be
correct.

About two decades earlier in 1895, German doctor H. A. Johne
was the first to describe the cause of a disease in cattle
characterized by chronic or intermittent profuse intractable
diarrhea.[30] Clinically, the
disease in cattle was virtually identical to that which we now know
as human Crohn's disease.[31] The
gross pathology of the infected cow's intestines likewise had the
same cobblestone appearance and microscopically, the Crohn's diseased
intestines and the diseased cattle intestines were dead ringers.[32] Dalziel wrote that the tissue
characteristics were "so similar as to justify a proposition that the
diseases may be the same."[33] He
theorized that the disease in cattle and the disease in people were
the same entity.

Mycobacterium paratuberculosis

The cattle disease, which became known as Johne's disease
(pronounced yo-neez), is known to be caused by a bacteria called
Mycobacterium paratuberculosis, also known as Mycobacterium avium
subspecies paratuberculosis, or MAP.[34] MAP belongs to an infamous class of microbes
called mycobacteria which cause diseases such as tuberculosis and
leprosy. In fact, before Johne properly distinguished MAP from other
mycobacteria, the disease in cattle was thought to be caused by
intestinal bovine tuberculosis, hence the name paratuberculosis or
"tuberculosis-like."

Mycobacterium paratuberculosis is one of the most enigmatic
bacteria known.[35] It lives inside
the hosts' cells, but has no known toxins and doesn't seem to damage
the cells.[36] The damage, much like
in diseases like hepatitis, comes from the hosts' reaction to it. MAP
triggers a massive immune reaction against the body's own tissues in
which MAP is hiding, in this case the gut.[37] It is known that M.
paratuberculosis--MAP--causes Johne's disease in cattle, but does it
cause Crohn's disease in people?

Spheroplasts

Paratuberculosis bacteria seem to cause disease in almost
every species of animal so far studied.[38] It's reasonable to assume the same might happen
in humans. ParaTB causes a specific chronic inflammation of the
intestines of cattle, sheep, deer, rabbits, baboons, and three other
species of primates.[39] The problem
for Dalziel was that he couldn't visualize the bug microscopically in
the surgically resected intestines of patients with Crohn's.[40]

While one can easily pick out MAP in most cases of Johne's
disease with a simple light microscope, to this day attempts to stain
and view MAP in Crohn's disease has been largely unsuccessful.[41] The landmark of most mycobacterial
infections is the presence of acid-fast bacilli, so called because
the mycobacterial cell wall soaks up and retains a particular acid
stain.[42] Although failure to see
acid fast bacilli in general is not uncommon,[43] in the intestines of Johne's disease infected
cattle, one can see swarms of acid-fast bacilli; in Crohn's there are
none. The mystery wasn't solved until 1984, when Rodrick Chiodini, a
microbiologist at Brown University's Rhode Island Hospital published
a landmark study in which he actually cultured live paraTB germs from
the gut walls of children with Crohn's disease.[44]

It has now been well established that paratuberculosis (and
some other mycobacteria[45]) can
shed their cell wall and exist as a what has been termed a "cell wall
deficient" or "spheroplast" form. Since it's the cell wall that picks
up the stain, this form of the bacteria cannot be detected using the
acid-fast stain test.[46] The bug,
however, can then reform its cell wall even years later and revert
back to its normal stainable self, which is what happened in
Chiodini's lab.[47] It is thought
that this cell-wall deficient form is responsible for triggering the
abnormal immune response which leads to Crohn's disease.[48]

Live Cultures

The next hurdle was the difficulty of consistently culturing
the bug from Crohn's sufferers' intestines.[49] Although MAP has been independently isolated
across three continents--cultured from Crohn's tissue in California,
Texas, France, Australia, England, the Netherlands, and the Czech
republic[50]--results are still
relatively sparse and many labs have reported not being able to
culture it at all.[51] This is not
surprising.[52]

In order to isolate a specific bug from the multitude that
exist naturally in the intestine, one has to devise a decontamination
technique that kills other bacteria without harming the target
bacterium, in this case MAP. Without it's protective cell wall,
however, cell wall deficient forms are almost impossible to culture
because of the caustic processing techniques required to isolate
them.[53]

Even once isolated, MAP is very difficult to grow.[54] Researchers have been trying since
1952 to grow mycobacteria from surgically removed Crohn's disease
tissue.[55] It is thought that
Chiodini succeeded where others had failed because of his many years
of experience, combined with access to modern culture techniques and
years of patient work.[56] Some
human isolates took up to six years to grow, even under extremely
precise culture and decontamination conditions.[57] Earlier researchers failed to meet these
stringent standards for culturing the bacteria.[58]

Even modern labs have been found to be relying on faulty
study design.[59] Moreover, the
differences in methods used between labs can be vast.[60] Some labs still use fixed or frozen specimens
or use only surface tissues from superficial biopsies, when it's been
shown that one should optimally use fresh[61] resected tissue, as MAP tends to be found deep
in the intestinal wall.[62] Some
labs working with nonspheroplast forms of MAP from cattle haven't
even been able to grow it. Even under the best circumstances, MAP is
a tough bug to grow.[63]

To this day, many infectious agents have eluded our attempts
to be grown in a lab at all. For example, scientists have never been
able to isolate Mycobacterium leprae, the microbe responsible for
leprosy. Even campylobacter, which we now know as the most
significant bacteria in food poisoning, wasn't identified as a human
pathogen until the 1970s, when culturing techniques enabling
isolation were finally developed.[64]

Complicating attempts to culture the bug in Crohn's, there
seem to be very few MAP actually involved in the disease process.
This has a parallel in other animals--MAP bacteria in sheep and goat
paratuberculosis are often sparse or even undetectable[65]--and in other mycobacterial human diseases like
a type of leprosy in which just a few mycobacteria are capable of
triggering a pathological immune response.[66]

DNA Fingerprinting

Obtaining Crohn's tissue samples is easy--patients are all
too frequently having pieces of their bowel removed--but growing MAP
from this tissue is so difficult that a non-culture based method was
needed. This advance came in the late 1980's when new DNA
fingerprinting techniques arrived on the scene.[67] Using DNA probe technology similar to that used
in forensic cases to pick up minute amounts of DNA, one can determine
the definite presence of paraTB without needing to actually culture
and grow it.[68] No longer would
researchers have to wait months or years for the spheroplasts to
revert back to normal and start growing again, one could just target,
with 100% certainty, MAP DNA.

Sixty-five percent of bowel samples from Crohn's patients
came up positive, compared to only 4% of those with the similar but
different disease ulcerative colitis.[69] As techniques for extracting and isolating DNA
have become better and better, MAP has been found in intestinal
Crohn's tissue with increasingly positive results.[70] The reason more Crohn's cases were not detected
is because the test has a limited sensitivity, especially when
searching for a needle in a haystack in the gut which is awash in the
DNA of billions of other bacteria.[71] DNA probe detection of other low abundance
bacterial pathogens, particularly in chronically inflamed
tissues--diseases like tuberculosis, Lyme disease, brucellosis and
lymphocytic leprosy--have similarly been fraught with difficulty.[72] Isolating chromosomal DNA from
mycobacteria in general is experimentally difficult.[73] There are also other substances in the gut that
have been found to inhibit the test such as bile salts and
polysaccharides.[74]

Also accounting for uncertainty in the data[75] is the frequent misdiagnosing of Crohn's
disease. For example, it's been shown that at least 20% of people
diagnosed with Crohn's actually have a different disease, such as
ulcerative colitis.[76] There is
also considerable debate on whether or not Crohn's is a single
disease entity in the first place.[77] Crohn's may be more of a catchall syndrome
describing a number of different conditions, some of which may not be
caused by MAP.[78] Either way, this
makes it difficult to interpret data that show that not all of those
we consider to have Crohn's disease test positive for MAP.

As expected, some people without Crohn's--healthy
controls--test positive. Yet just because someone comes in contact
with and harbors a specific germ doesn't necessarily mean that person
will come down with the disease.[79]
It is estimated, for example, that only 1/3 of calves that ingest MAP
ever develop Johne's.[80] It is also
possible, like closely related subspecies, that there are different
strains of MAP, some of which cause disease and some of which
don't.[81] The important point is
that there has consistently been a highly significant specific
association between Mycobacterium paratuberculosis and Crohn's
disease.[82]

Association or Causation?

Just because Crohn's sufferers are much more likely to have
MAP found in their gut does not necessarily mean that MAP caused the
disease. Another explanation of the finding could be that this is
just an opportunistic invasion of MAP into diseased tissue, leading
to a chicken and egg scenario of which came first.[83] If MAP just has an affinity for inflamed
tissue, however, one would expect that one would also find MAP more
frequently in biopsies of similar diseases like ulcerative colitis,
but this is not the case. Conversely if you look for the DNA of other
nonspecific mycobacteria, one finds that they are uniformly
distributed between Crohn's patients versus controls. This finding is
consistent with the known environmental distribution of mycobacteria,
which are present in 30-50% of all environmental samplings--including
water, soil, even air.[84] So other
mycobacteria people routinely come in contact with, even the closely
related Mycobacterium avium subspecies silvaticum, are equally
distributed among people whether they have Crohn's disease, or colon
cancer, or are completely healthy as one might expect.[85]

In medicine there is a method used to try to prove that a
specific pathogen causes a specific disease. The first person to
definitively prove that a disease was caused by a particular organism
was Robert Koch, who uncovered the bacterial origin of anthrax in
1876. Koch cultured the bacteria from a diseased animal, gave anthrax
to a healthy animal by inoculating her or him with a pure culture of
the bacilli, and then was able to recover and reculture the bug once
again.[86] These experiments
fulfilled criteria proposed 36 years earlier by Henle as necessary to
establish a causal relation between a specific agent and a specific
disease. These criteria are now known as the Koch postulates.[87]

Not only are these experiments arguably unethical,[88] they also can be unreliable in
clinical medicine, as other animals may not be susceptible to the
same diseases that we are. For example, the case to prove that H.
pylori caused ulcers was hindered by animal research, as rats and
pigs were tested and seemed to be immune.[89] For this and other reasons, there are some
recognized infectious diseases which have never fulfilled Koch's
postulates. Leprosy, for example, has still never fulfilled more than
one of the four criteria, because it is not possible to culture the
culprit bacterium in the laboratory. Nonetheless, Mycobacterium
leprae is known to be the cause of leprosy, and leprosy is known to
be an infectious disease.[90] So
while not absolutely necessary to fulfill Koch's postulates to prove
causation, they are the most widely accepted method. So researchers
set out to the task and they succeeded--twice.[91]

Chiodini fed chickens pure cultures of the paratuberculosis
bacteria he recovered from the surgically removed intestines of
children with Crohn's disease. The chickens then developed an
intestinal disease resembling Crohn's.[92] In 1986, a different lab fed infant goats a
human strain of paratuberculosis and also found that the bacteria
induced a Crohn's-like intestinal disease in the goats. The same
strain was then recovered back from all of them.[93] When asked why there continues to be so much
resistance against the idea of MAP as a cause of Crohn's disease,
Chiodini replied "What you have to realize is that there is a lot of
politics in medicine. It's not whether you have the proof of
something, but whether or not the medical community wants to accept
it."[94]

Because there have been so many other failed attempts to
figure out the cause of Crohn's, the medical community is very leery
of new proposed causes, especially infectious ones.[95] The gastrointestinal community maintains a
healthy skepticism regarding new pathogens as the cause of Crohn's
disease, because different pathogens suspected in the past, such as
chlamydia and measles, have since been disproven.[96] Of all the pathogens once thought associated
with Crohn's in the 80 years it's been researched, MAP is the only
one directly cultured and the only one capable of causing
pathologically indistinguishable disease in other animals.[97]

The way that doctors test for the presence or absence of many
infectious diseases is by looking for specific antibodies that our
immune system uses to target the invader. When we test for HIV, for
example, we are not usually testing for the virus directly, we are
looking for the presence of anti-HIV antibodies.[98] If they're found, we can be relatively certain
the person has been exposed to HIV. Similar searches have been
launched for anti-MAP antibodies. Unfortunately scientists have had
difficulty finding an antibody which is specific for MAP.[99] There are some promising new
suspects, however, which are thought to be unique to MAP and have
been found in 90% of Crohn's patients, but in less than ten percent
of those with ulcerative colitis.[100] These results not only support the theory,
but open new research frontiers. A vaccine might be developed and the
diagnosis of Crohn's may soon be just a blood test away.[101]

Epidemiology

Other potential lines of evidence include population studies.
One would expect that if paratuberculosis was causing Crohn's disease,
then the regions in which there is a high prevalence of Crohn's
should overlap with the regions with a high prevalence of
paratuberculosis. While sufficient data is lacking,[102] a review of the epidemiology of Johne's
disease compared with the epidemiology of Crohn's disease found just
that.[103] "Crohn's disease has a
very spotty distribution in the world," notes Dr. Walter Thayer, an
expert on the disease at Rhode Island Hospital who worked with
Chiodini to culture MAP from Crohn's patients. "But it's seen only in
milk-drinking areas--Australia, southern Africa, Europe, the United
States, Canada, New Zealand. Interestingly, it's not seen in India,
where they do drink milk, but they boil it first."[104]

Critics point to Sweden, which has its share of Crohn's, but
whose cattle are reportedly paratuberculosis free. Unfortunately, the
surveillance testing has been limited.[105] Michael Collins, veterinarian and
microbiologist with the University of Wisconsin, has written "We
believe no region in the world is free of M. paratuberculosis
infection in its ruminant livestock. In all likelihood, Johne's
disease is to be found in every country. Being free of the disease is
probably more a function of how hard one has looked than a true lack
of incidence."[106] We will see a
prime example of this in the discussion of Ireland.

Another perceived inconsistency in the link between paraTB
and Crohn's is the fact that Crohn's is found more often in urban,
rather than rural populations.[107] Dairy farmers, for example, do not seem to
have higher rates of Crohn's.[108]
This is not dissimilar from other parallel diseases like bovine
TB--tuberculosis not paratuberculosis--which, centuries ago, was
responsible for the deaths of hundreds of thousands of children who
drank unpasteurized milk.[109] The
association between tuberculosis contracted by drinking milk and the
rural community was also weak, presumably because of the commercial
marketing and distribution of infected milk.[110]

Any explanation of Crohn's would have to account for the
rapid increase seen in this disease this century.[111] The longest continuous study of the incidence
of Crohn's disease is from Wales, which reports a 4000% increase of
the disease since the 1930's.[112]
This may be explained by the concurrent rise in paratuberculosis in
intensively farmed dairy herds throughout the century.[113] Thayer asks also "What has
happened to dairying in that time? Do you get milk from your local
dairy? No. You get it from big conglomerates that buy from local
dairies and pool all the milk. I think this is possibly the reason
the disease has spread so quickly."[114]

Nick Barnes

Two centuries ago, when milk drinking children were dying en
masse from bovine TB, one of the earliest signs that they had drunken
milk from a tuberculous cow was an infection of the lymph nodes that
drained the throat. Scientists think milk is also the source for
human exposure to paratuberculosis, so they wondered if the same
thing happened with MAP.

Enter Nick Barnes, a 7 year old boy who developed a painful
swollen lump on the right side of his neck. His family took him to
see their doctor, who decided it needed to be biopsied. The biopsy
clearly showed he was infected with paratuberculosis. This is
significant because it was the first definitive proof that
paratuberculosis could infect human beings and cause disease. He and
his family waited. Five years later, Nick Barnes came down with
Crohn's disease.[115] Despite the
clear cut case description of a human paratuberculosis infection
followed by the development of Crohn's, the medical community
continued to ignore the growing evidence indicting MAP. There are
many precedents of similar resistance to new ideas in the medical
field.

H. pylori

Most ulcers are caused by the immune system attacking the
lining of the stomach. Doctors blamed stress, thinking this led to
too much stomach acid and the excess acid caused irritation which
maybe triggered the attack. It was treated the same way as Crohn's
has been treated: symptomatic relief of the inflammation and surgery.
Then two Australian researchers cultured a tiny bacterium from the
lining of the stomach and hypothesized heresy--that ulcers were
actually caused by an infection.[116]

For almost a decade the researchers' ideas were dismissed and
ridiculed.[117] The medical
community scoffed at the notion that bacteria could survive in
stomach acid.[118] One of the
Australian researchers was so desperate that he actually drank a vial
of the bacteria to prove his point.[119] What finally convinced the medical community,
though, was that ulcers disappeared when patients were treated with
the right antibiotics.[120] This
discovery revolutionized thinking in medicine. The ulcer-causing
bacteria, H. pylori, is now known as the cause of most ulcers in the
world.[121]

Many scientists see a close parallel between the H. pylori
story and paraTB. Just as H. pylori bacteria were the real reason the
body was attacking the stomach lining in ulcers, researchers think
that the MAP bacteria are the reason the body is attacking the
intestinal lining in Crohn's. The proposition that ulcers were an
infectious disease was met by nearly universal skepticism in the
medical community.[122] As Dr.
Hermon-Taylor, Chairman of the Department of Surgery at St. George's
Medical School in London and leading proponent of the paraTB-Crohn's
link, has noted, "And this [H. pylori] was a bug that you could see
by looking down the microscope, grow in a simple culture system in
the lab, test for immunologically pretty simply, and ordinary tablets
readily available to doctors could make it go away. And it still took
eight years for the penny to drop. Now we've got a bug [MAP] that you
can't see, can't grow, hides under the immunological radar, is a
bastard to kill, and the problem it's causing is far, far greater. If
Rod Chiodini and I are wrong, the magnitude of the problem will only
be the economic losses of farm animals, which is costing the US
somewhere between $1.5 and $2 billion a year. If Rod Chiodini and I
are right, then, oh dear, oh dear. We have a big problem. It's going
to take a lot to put it right."[123]

Antibiotics for Crohn's

The lesson researchers learned from stories like H. pylori[124] was that their best bet at
convincing the world that MAP causes Crohn's lay in trying to cure
Crohn's--a disease thought incurable--with appropriate antibiotics.[125] Of course there was no
guarantee that even if the disease were caused by MAP that it would
respond to treatment.[126] For
example, we can cure most pulmonary TB with antibiotics, but when TB
bacteria move from the lung to the intestine and cause intestinal TB,
it cannot typically be cured by antibiotics alone.[127] Researchers, though, set out to try.

Before we knew that ulcers were treatable with simple
antibiotics, people underwent repeated grueling surgeries--some
almost as risky and debilitating as Crohn's sufferers now undergo.
Not only would a cure save Crohn's sufferers from the surgeon's
knife, but it would also protect them from the toxic chemotherapy regimens
currently used just for symptom relief, which can include
immunosuppressants like steroids, cancer chemo agents[128] and even thalidomide.[129]

Researchers started trying antibiotics they thought might
kill MAP in Crohn's. Early results were disappointing,[130] leading to much of the
deep-seated resistance among clinicians to accepting MAP as the cause
of Crohn's.[131] Yet in hindsight,
it turns out tht doctors were using the wrong antibiotics, in the
wrong combinations, for an inadequate period of time.

Perhaps because of the name similarity, many researchers
assumed that antibiotics effective against M. tuberculosis should
also be effective against M. paratuberculosis.[132] They were wrong; when one actually tested
antibiotics against MAP in a lab, researchers found that it was in
general resistant to anti-tuberculous drugs.[133] They didn't work in cows[134]; they don't work in people.[135]

Another problem with some early studies was that they used
monotherapy--meaning that they only used a single agent--which is
rarely, if ever, effective in mycobacterial diseases because
mycobacteria are so adept at developing resistance.[136] By giving multiple antibiotics at once, one
decreases the chance that resistance will develop.

Adequate treatment duration had also been neglected.
Mycobacterial infections in general are difficult to eradicate;
prolonged treatment is required and relapses, either on treatment or
off treatment, are common.[137]
Tuberculosis takes months to treat; leprosy takes years--sometimes a
lifetime--to treat. Our best estimate of how long it might take to
rid the body of MAP can be made by studying pathogens in the same
species. Infections caused by one of MAP's closest cousins routinely
require treatment for 3-4 years with 3 or 4 different antibiotics.[138] In some cases, it took five
antibiotics all used in combination for 5 years before clinical
improvement was achieved. We cannot expect trials using too few
drugs, the wrong drugs, or even the right drugs for too short a time,
to be successful.[139]

There are some factors which complicate any trial, even if
the agents are chosen and used appropriately. Crohn's can be a
cyclical disease, with periods of flare-ups and remissions, so
approximately 20% of Crohn's patients during a treatment period will
spontaneously improve on their own. The placebo effect is also
expected to play a role in 30-40% of patients undergoing short-term
therapy. And as mentioned previously, Crohn's is a poorly delineated
disease--20% of people diagnosed with Crohn's may actually have
something else.[140] There is also
clinical, epidemiological, and molecular evidence indicating that
there are two distinct clinical manifestations of Crohn's disease,
which each may respond differently to treatment. These factors make
it difficult to evaluate any therapeutic intervention.[141]

Despite these hurdles, the latest results are quite
promising,[142] Instead of just
blindly trying different antibiotics, scientists actually endured the
laborious task of testing the antibiotics one by one on MAP in the
lab. The breakthrough came in 1992 when the newly developed
antibiotic clarithromycin was found to be the most effective known
killer of Mycobacterium paratuberculosis. Many of the antibiotics
used earlier worked by blocking cell wall synthesis. But Crohn's is
thought to be caused by the spheroplast form of MAP which doesn't
have a cell wall; it's therefore no wonder these earlier drugs didn't
work. Clarithromycin, and an antibiotic called rifabutin, have a
different mechanism of action, blocking protein synthesis.[143]

Another reason why drugs like clarithromycin (called
macrolides) work against paraTB where others have failed is that MAP
is an intracellular pathogen. They live inside our cells (another
reason why they're so hard to see under a microscope). Only certain
antibiotics, like macrolides, can penetrate inside human cells and
still work effectively.[144] None
of the previous MAP trials properly evaluated these newer macrolide
antibiotics.[145] The time was
ripe for a trial of these newer agents in Crohn's disease.

An Attempt at Cure

The first trial took place in London, published 1997.[146] Researchers chose to use
rifabutin and clarithromycin because they seem to complement or
synergize with each other.[147]
The treatment was named RMAT, Rifabutin and Macrolide Antibiotic
Therapy.

Fifty-two patients with Crohn's disease, most of whom had
persistent severe symptoms resistant to conventional treatment, were
studied. Six patients had to be excluded, due mostly to intolerance
to the antibiotics,[148] though in
general the RMAT medications tend to have a much higher tolerance
rate and far fewer side effects than the current immunosuppressive
drugs used for Crohn's.[149] The
remaining 46 patients were treated with RMAT for about a year. Of the
46 patients who were able to tolerate RMAT, 43 went into clinical
remission, for a remission rate of 94%.[150]

A two-year follow-up was performed. The majority of patients
in whom a clinical remission was initially induced remained symptom
free off of all their previous medications.[151] Similar trials in other centers have
reproduced these findings.[152],[153],[154],[155],[156] The fact that some patients
relapsed after treatment was stopped may point to the difficulty in
eradicating the organism or perhaps that they had been re-infected.[157] Hermon-Taylor, one of the
principal investigators of the original trial, is currently
recommending patients take RMAT regimen for at least 2 years. Among
patients who respond to treatment, remission occurs slowly over the
first three to six months of treatment. Symptoms often get worse
before they get better, as in the drug treatment of other chronic
mycobacterial diseases such as leprosy.[158]

Based on this pilot study, RMAT has the highest reported
remission rate of any known treatment for Crohn's disease and the
lowest reported relapse rate, including all current immunosuppressive
treatments.[159] Thought to be an
incurable disease, doctors seem to have been able to induce profound
long-term remissions in the majority of patients with Crohn's
disease.[160] Not only do patients
stop having symptoms, but their intestines actually show evidence of
healing, an unprecedented achievement.[161] "If this were cancer," said one RMAT
researcher, "we would be calling these long remissions a cure."[162] Hermon-Taylor told the press
"I've seen people who were without hope get better like magic. I've
been a doctor for nearly 40 years, and it's the best thing I've ever
seen in clinical medicine."[163]

Though the preliminary results of this and other pilot
studies are encouraging, Hermon-Taylor is the first to point out the
limitations of the study--it was too small and there were no
controls.[164] "We were actually
denied the funding to do a randomized control trial," he said. "So I
did the best that I could with what I've got."[165] To date, according to the Cleveland Free
Times article that won 1999's Project Censored Award, twenty-five
of Hermon-Taylor's grant proposals submitted both here and abroad
were rejected.[166]

Chiodini estimates he's similarly submitted over two dozen
grant proposals to the National Institutes of Health, the USDA and
the Crohn's and Colitis Foundation of America, but to no avail.[167] Drugs trials run in the United
States have traditionally been supported by the pharmaceutical
industry, but just as H. pylori threatened to deprive some of the
largest corporations in the world of billions of dollars (anti-ulcer
medications were the world's best-selling prescription drugs), the
drug industry scores huge profits from increasingly complex and
expensive maintenance Crohn's treatments, which must be administered
for the rest of the patient's life.[168] Needless to say, financial support from the
corporate sector has not been forthcoming.[169]

Nevertheless, these preliminary results must be reproduced to
be seriously considered. Larger scale controlled studies are
currently in progress to obtain better data.[170] The most promising is a phase III clinical
trial of RMAT in Australia which has been designed as a double-blind,
multi-center, controlled clinical trial involving over 200 patients
with Crohn's in at least seven major cities across the continent.[171] Unfortunately, they seem to be
having a problem securing patients for the study.[172] A controlled RMAT trial has also reportedly
been initiated by the National Institutes of Health.[173]

Milk and Pus

Professor Hermon-Taylor, internationally known expert on
Crohn's and MAP genetics, who has researched the illness for 20
years, said: "If there were no MAP I believe there would be almost no
Crohn's disease. It is certainly responsible for between 60 per cent
and 90 per cent of all cases and I would think that it is more likely
to be 90 per cent."[174]
Obviously, everyone who's exposed to paraTB doesn't come down with
Crohn's disease, as is the case in virtually all infectious diseases.
As mentioned previously, just because one comes in contact with a
pathogen does not necessarily mean one comes down with the illness.
Genetic and environmental factors facilitate establishment,
persistence, and production of disease.[175]

H. pylori, for example, (the bacterium proven to cause
ulcers) is one of the most common of all bacterial infections[176]--a third of Americans have H.
pylori in their stomachs.[177] A
third of us, however, don't have ulcers;[178] some people are just susceptible. Similarly,
only about one in three hundred people exposed to tuberculosis
actually come down with active disease.[179] Until we know why some and not others fall
ill, all one can do is to try to minimize exposure to the pathogen.
For example, people should not let those with tuberculosis cough in
their face.

Drinking milk from cows infected with Johne's disease is how
people are exposed to paratuberculosis. Based on DNA fingerprinting
techniques, there are two strains of MAP: one that affects cattle,
and one that affects goats and sheep. All human isolates so far have
been of bovine origin,[180]
implicating milk.[181] Milk is the
"logical" focus of exposure[182]
because cows with Johne's disease secrete paraTB abundantly in their
milk.[183] Even sub-clinical
cows--those that are infected but appear perfectly normal--shed
paraTB bacteria into their milk.[184] Although these bacteria are found
free-floating in milk, their transmission may be facilitated by their
presence inside pus cells.[185]
This is a particular problem in the United States, as we have the
highest permitted upper limit of milk pus cell concentration in the
world--almost twice the international standard of allowable pus
cells.[186] By US federal law,
Grade A milk is allowed to have over a drop of pus per glass of
milk.[187] These pus cells may
facilitate the transmission of paraTB.[188]

Pasteurization

In England, researchers took milk off grocery shelves and
tested it for the presence of paratuberculosis bacteria using DNA
probes. Depending on the time of the year, up to 25% of milk cartons
contained paratuberculosis DNA.[189] Interestingly, the seasonal variation
coincided with the periods when Crohn's patients tend to suffer
relapses.[190] The researchers
tried to culture live paraTB bugs from the milk, but were largely
unsuccessful, because cow's milk is such a stew of microbes that
fungal overgrowth and faster multiplying bacteria took over the
samples.[191] The question then
remained, did the positive DNA samples in up to a quarter of the milk
supply indicate live or dead paratuberculosis bacteria? Can paraTB
survive pasteurization?

Historically, pasteurization had been established in order to
kill paraTB's cousin, bovine tuberculosis.[192] TB was thought to be one of the most heat
resistant human pathogens, so the temperature was set at
approximately 62o Celsius (144o Fahrenheit) for a half an hour.[193] Later, the disease Q fever was
discovered, so the temperature was increased to 63o Celsius.[194] Now the HTST method, which
stands for High Temperature, Short Time, is predominantly used--72o
Celsius (162o F), but only for 15 seconds.[195] While 72o C kills most bacteria,
paratuberculosis has been shown to survive 15 seconds at 90o Celsius
(194o F).[196] By hiding in milk
in fat droplets, pus cells, and fecal clumps,[197] paraTB might be able to survive at even
higher temperatures.[198] Second
only to prions[199] (which cause
mad cow disease), paratuberculosis is considered the most heat
resistant pathogen in the human food supply.[200]

Johne's on the Rise

According to the Food and Agriculture Organization of the
United Nations, Johne's disease is one of the most serious diseases
affecting the cattle industry.[201] Although it is found in cattle populations
throughout the world, the United States appears to have the worst
paratuberculosis problem on the planet.[202] In 1997, the USDA released a long-awaited
report of the national prevalence of Johne's disease. Surveying over
2500 dairy producers,[203] they
showed that between 20-40% of US dairy herds were infected, a figure
that they concede is probably an underestimate.[204] Since milk from an entire herd is likely to
be pooled together in tankers for transport to processing plants, the
20 to 40% figure is likely to indicate the level of contamination in
American milk.[205]

Just as Crohn's disease is increasing in the human
population--it may be no coincidence that the US also has the world's
highest incidence of Crohn's ever recorded[206]--Johne's disease is spreading among dairy
cattle.[207] Johne's disease is
spread primarily by the fecal-oral route. One can imagine how a cow
with intractable diarrhea can thoroughly contaminate her
surroundings[208] and just a few
bits of swallowed manure can potentially infect a calf.[209] Overtly infected animals,
losing up to 300 lb. of body weight in one week[210] can shed as many as ten hundred trillion bugs
a day.[211] One can also imagine
what intensive modern farming practices have done for the disease.[212] Grazing bigger and bigger
numbers of cattle on smaller and smaller plots of land is one of the
reasons this dreaded disease is such a growing threat.[213] And every time animals are
transported between farms, new herds may be infected. If no changes
are made, the dairy herd infection rate is expected to reach 100%.[214]

USDA Farce?

With the growing Johne's epidemic, US governmental regulatory
agencies have been in a bind. The only thing allegedly standing
between people and the paratuberculosis bacterium are 15 seconds at
72o Celsius.[215] The government
has had to somehow convince the families of Crohn's patients who
started to ask questions that pasteurization was foolproof. The
problem was that the preponderance of the scientific evidence was
against them--almost every study ever done simulating pasteurization
conditions showed that paraTB survived the 15 seconds at 72o C.[216] So USDA scientists designed
their own experiment.

Critics accuse the USDA of trying to ensure that no paraTB
would survive in their pasteurization experiment by first crippling
the bacteria. Very irregularly, with no precedent in the scientific
literature for using this type of approach,[217] the USDA began their experiment by first
"starving" the MAP bacteria,[218]
exposing them to high-frequency sound waves, and freezing them--a
technique that has been shown conclusively to weaken MAP.[219] They were also criticized for
making a number of methodological mistakes and omissions.[220],[221] Then, allegedly to make absolutely sure not a
single bug would grow, they used an inadequate culture media[222] and report culturing them for
only 2 to 3 months.[223] It is
widely accepted that the minimum time it takes to ensure the growth
of paraTB is 4 months.[224]

It is perhaps not surprising that no MAP grew from the
pasteurized milk in their experiment. The researchers concluded:
"Results indicate that the transmission of live paraTB bacteria via
pasteurized milk is unlikely." Despite fifteen[225] years of better research to the contrary,[226] based on that single
questionable study, in a letter dated Feb. 9, 1998, Joseph Smucker,
the leader of the FDA's Milk Safety Team wrote "After a review of the
available literature on this subject, it is the position of FDA that
the latest research shows conclusively that commercial pasteurization
does indeed eliminate this hazard."[227]

The FDA has argued that earlier pasteurization studies used
unrealistically high levels of MAP that wouldn't be expected to exist
naturally in the raw milk supply.[228] This is not a tenable criticism, primarily
because the studies in question followed the published guidelines on
the proper challenge concentration in the design of thermal
inactivation studies.[229] Also,
the concentration of MAP in raw milk is unknown. Cattle infected with
Johne's disease have uncontrollable diarrhea, which "sprays" out from
them in liquid form. Due to the close proximity of the cow's anus to
her udders, it is unavoidable that an infected cow's udders will be
smeared with feces, potentially leading to the contamination of her
milk with high numbers of Mycobacterium paratuberculosis.[230] The feces contaminating her
milk can have as many as a trillion paraTB bugs per gram.[231]

Off the Shelf

Despite its shortcomings, the USDA study continues to be
cited and the rest of the scientific literature ignored by the
government and the agricultural press.[232] Hoard's Dairyman, for example, cited the USDA
study and concluded that "pasteurization destroys this dangerous
disease."[233] It wasn't until the
year after the study was published that such assertions were proven
to be wrong.

The only way to demonstrate for sure that live paraTB
bacteria survive pasteurization is to culture a colony of living
paratuberculosis bacteria from retail pasteurized milk off the
grocery shelf. In 1998, that is just what researchers did. Choosing
Ireland, which has the highest per capita milk consumption in the
European Union,[234] investigators
went to 16 retail outlets and got 31 cartons of milk which were
pasteurized at commercial dairies large and small.[235] Six grew out live paraTB, 19%--almost 1 in
5.[236] This caused a national
food scare with daily front page headlines, not a word of which
crossed the Atlantic.

In an editorial entitled "Media and Censorship," the
Editor-in-Chief of the Cleveland Free Times wrote "The dairy lobby is
notoriously powerful inside the Washington D.C. beltway. And a tax
on dairy farmers helps the dairy industry spread its advertising
dollars around generously (most notably the 'Got Milk?' ad campaign),
to the point where the wholesomeness of milk goes virtually
unquestioned in the media. How else can it be explained that the
possible link between a bacterium in milk and Crohn's disease is
virtually unknown in the United States, despite front-page coverage
in England and other places around the world."[425]

When the results of the Irish study were released, crisis
management specialists called the ramifications "enormous,"
"horrific." Dairy industry experts described it as a "significant
blow to the industry," "accelerating the long-term decline of milk,"
and noting "It's not a market that can just bounce back."[237] Dairy industry leaders reacted
angrily to the suggestion that pasteurization was inadequate. The
British National Dairy Council's "Information Officer," said she
wished the investigators had contacted the industry before publishing
their scientific findings.[238]

Responding to public pressures, the British government
initiated a nationwide thousand-sample survey of retail pasteurized
milk. The announcement splashed headlines all over Europe, but there
was still no word in the American press.[239] The preliminary findings of the British
government's survey were released in April, 2000. Three percent
NAME="fnB240" HREF="#fn240">[240]--3 out of every one hundred
cartons of milk off the shelves--grew out live paratuberculosis
bacteria,[241][242] Based on the detection
threshold of these tests, each quart had to contain at least about a
million paraTB germs to come up positive.[243]

A year and a half earlier, after the announcement that milk
was contaminated by at least paraTB DNA, the three British
supermarket giants--Tesco, Sainsbury and Safeway--announced that milk
pasteurization time would be increased from 15 seconds to 25 seconds,
to reassure the public that their products were safe.[244] The finding of live paratuberculosis bacteria
in retail milk over a year later has fueled the skepticism that the
10 second change would make any difference.[245] The change was not based on science--in fact
there is a suggestion that some paraTB can survive pasteurization
temperatures for 9 minutes[246] or
longer.[247]

Public Relations

Despite the release of these findings, the British
Agriculture Minister said on national television: "I drink
pasteurized milk and it is safe to do so... with confidence," a claim
reminiscent of a previous Minister's assurances about beef from
cattle infected with mad cow disease.[248] According to the Royal Statistical Society,
contaminated beef still has the potential of killing 13 million
people who consumed it and are currently incubating the disease which
Britain's Health Secretary called the worst form of death
imaginable.[249]

The same assurances are echoed in the US. For example, the
director of the USDA National Animal Disease Center, feeling assured
that pasteurization eliminated any health threat said, "I don't
hesitate to feed [milk] to my 8-year old."[250] The FDA chooses to continue to base national
safety policy on the single flawed USDA study,[251] even now that it's been superseded by proof
that its conclusions are wrong (the US mandates the same
pasteurization method that is used in Britain and Ireland).[252]

The FDA's continued insistence that pasteurization eliminates
the risk of contracting paraTB--despite clear evidence to the
contrary--puzzled Kurt Gutknecht, the editor of the highly respected
industry publication Wisconsin Agriculturist. He called up Joe
Smucker, the leader of the FDA's Milk Safety Team, and asked him
about the FDA's official "commercial pasteurization does indeed
eliminate this hazard" statement. Smucker replied that he did not
have "clearance from the FDA" to speak to him on the subject.
Surprised at Smucker's reluctance to talk to him, the editor went to
the official FDA spokesperson, who described the refusal of an FDA
official to not respond directly to press inquiries as "very
unusual." Gutknecht turned his attention back to the Milk Safety Team
which no longer returned his phone calls.[253]

The industry and/or[254]
government knows, however, what kind of time bomb they're sitting
on.[255] According to one industry
expert, the incrimination of MAP in human disease would cause
enormous economic damage to animal agriculture industries. An article
in Milk Science International entitled "Mycobacterium
paratuberculosis: A possible agent in Crohn's Disease?" warns that
"the present state of knowledge is... potentially catastrophic for
the dairy industry should existing information be used in a
sensationalist manner."[256]

Hidden Threat

Johne's disease is one of the most difficult diseases to
recognize and control.[257] This
is in part because of MAP's ability to resist destruction in the
natural environment. It has reservoirs in pasture and, perhaps, in
other animal populations. Paratuberculosis has spread, for example,
from dairy cattle to wild free-ranging white tailed deer in the state
of Connecticut.[258] The chief
reason that paraTB is so hard to prevent and control, however, is its
notoriously covert nature.

Paratuberculosis has been called a "spectral disease,"[259] a "hidden threat,"[260] an "insidious problem for the
nation's dairy herds."[261]
Although infections are usually initiated during calfhood, clinical
disease does not appear until adulthood.[262] During this incubation period, which can last
between 6 months[263] and 15
years,[264] the infection is
invisible.[265] Sub-clinically
infected animals don't have diarrhea or other typical visible signs
of Johne's, but they are carriers and can shed the bacteria into the
environment, giving paraTB ample opportunity to become entrenched in
a herd before it is apparent that a problem even exists.[266]

In this way, the Johne's disease problem has been likened to
the tip of an iceberg--the so-called "iceberg effect."[267] By the time a single clinical
case surfaces, five[268] to
fifteen[269] or twenty[270] others may be infected in the
herd. If the clinically affected animal had been born on the farm, a
minimum of 25 other animals are probably infected--perhaps as many as
50--and less than 30% of those would be detectable by currently
available tests.[271]

Johne's may also be clinically hard to detect. While in some
instances the disease progresses relatively rapidly, with the
interval between the appearance of wasting and death measured in
months, in other cases, after the initial loss of condition, there
may be no clinical deterioration for long periods of time. Since the
first signs of clinical disease are progressive weight loss and a
drop in milk production, farmers may just cull the animal without
requesting further diagnosis.[272]
Also, like Crohn's, Johne's can go into periods of remission which
can last for weeks or even months.[273] Finally, Johne's can mimic other diseases
like intestinal parasitism, malnutrition, salmonellosis, winter
dysentery, etc.[274]

Traditional control methods have involved culling infected
animals and using hygiene methods to prevent new infections.[275] Removing infected animals alone
has proven ineffective because of the latency period and because the
bacterium survive so well outside the body. As one commentator noted,
"An iceberg is not destroyed by the removal of the tip!"[276] Another proposal has been to
kill off the entire herd, an option termed "herd disposal." The plan
would then be to disinfect the barns and wait a year or so before new
animals are allowed to pasture. This measure will likely never be
initiated, though, because paraTB is so widespread that the resulting
financial burden would be considered too great.[277]

After culling, the next most effective action is considered
to be segregation of the infected animals.[278] Strict hygiene, down to the washing of boots,
is necessary to prevent cross contamination--only a few grams of
manure are needed to infect a calf.[279] Surveys show that many of these basic steps
are not followed, however. For example, in approximately a third of
operations, the cows' udders are not routinely washed prior to
collecting colostrum or before nursing.[280]

While some calves are infected in utero,[281] removing newborn calves from the mother
immediately upon birth is considered an effective control measure
because it eliminates the newborn's attempt to nurse and risk
ingesting infectious manure.[282]
Currently, about two thirds of dairy operations report taking the
calf away from the mother within 24 hours.[283] There are fears among the animal welfare
community that Johne's disease management will intensify this
irresponsible[284] practice.

Disposal of infectious feces creates a quite a problem. Some
industry specialists have advocated special landfills, while others
have made the potentially hazardous proposal to "as a last resort,
spread [it] on permanent crop land."[285]

Conspiracy of Silence

Despite its pervasiveness and its ability to severely impact
milk production and destroy whole herds of cattle, Johne's disease
remains an industry problem that is not openly discussed.[286] In an article entitled "Johne's
Disease: a Dairy Industry Perspective," Johne's is described as
"Something that farmers talk about secretly--whisper behind hands."
One dairy scientist stated that in all his years he had never heard
an open, frank discussion of Johne's disease and calls for end of the
"whispering campaign."[287] Dairy
farmers try to hide the fact that they have the disease in their
dairy herds.[288] As an article in
Cornell Veterinarian notes, "Farmers prefer not to acknowledge
its presence and enshroud suspect cases with secrecy."[289] It is a problem that is kept
out of sight and out of mind. As one dairy farmer put it "It's
[Johne's] a dirty word. It's like AIDS--you don't talk about it."[290]

This conspiracy of silence extends beyond the producers to
encompass the entire industry to the point of interfering with
scientific dialogue.[291] From the
Journal of Dairy Science: "Fear of consumer reaction... can
impede rational open discussion of scientific studies."[292] Without doubt, says Chiodini
"the dairy and regulatory industries are concerned vocally... but
their concern is limited to the possibility of 'bad press' to the
industry rather than a concern for the truth or public health."[293]

The secrecy has successfully bred ignorance. Over a century
after the disease was identified, almost half of all dairy farmers
nationally surveyed by the USDA didn't know anything about the
disease.[294] And those with the
largest herds--the herds most likely to be infected[295]--were found least likely to have known of the
disease.[296] Karen Meyer, then
Executive Director of the nonprofit Paratuberculosis Awareness and
Research Association (PARA), placed the blame on the representatives
of the dairy industry. At a meeting of the USDA's United States
Animal Health Association (USAHA), she challenged dairy producers to
become more proactive. "If there are organizations you have been
relying on for your information and to protect your interests, they
have failed you miserably."[297]
"I think we underestimate farmers," she told the Wisconsin
Agriculturist. "If they even thought they were making someone
sick, it would break their hearts."[298]

US Inaction

The USDA has been accused of continuing to keep its head in
the sand. Industry specialists blame the federal government for
"grossly underfunding" research, with less than one percent of its
animal disease grant budget allocated to Johne's.[299] As Alan Kennedy, a co-founder of PARA and
himself a sufferer of Crohn's disease remarked, "yet another case of
CJD--Conflicting Job Description." The USDA is mandated to regulate
animal industries and food safety, but it is also responsible for
promoting these same agricultural products.[300]

The first US case of Johne's was discovered in Pennsylvania
in 1908.[301] Almost a century
later there is still no mandated control program,[302] even though as far back as 1922 scientists
published warnings of the danger posed by the disease and outlined
effective methods of controlling and eradicating it. Efforts to
control and eradicate Johne's disease have been grossly inadequate.[303] "In the 75 years following the
release of that publication, there's very little that any state has
done to try to control the disease," says Collins, the University of
Wisconsin veterinary researcher. Meanwhile, as predicted in 1922, the
disease has continued to spread silently and surely. According to the
USDA's figures, there are now three quarters of a million cattle
infected with paraTB in the United States.[304]

The reason that Johne's has spread to such a degree is
because there have been no direct constraints on the transport of
infected animals.[305] Almost
without exception, paratuberculosis is introduced into a herd through
the addition of an asymptomatic infected carrier animal. Almost every
infected herd can trace the infection to the purchase of an infected
cow[306] that appeared healthy
when offered for sale.[307]
Disturbingly, the USDA found that dairy farmers with infected herds
were no less likely to sell replacement cows to other farms than
owners of noninfected herds.[308]

Regulatory vets know and accept this fact, acknowledging that
movement restrictions on infected animals must exist for an effective
control program. However, as described in the Veterinary Clinics
of North America , "if the voluntary program imposes movement
restrictions, it could quickly become a regulatory program and not
have widespread support and participation from the livestock
industry."[309] In fact the Code
of Federal Regulations (part 80) was recently changed to remove
restrictions on the interstate movement of Johne's disease positive
animals.[310] The change was made
because of pressure from the livestock industry.[311]

Though not putting its money where its mouth is, the USDA
insists that the agency is doing everything it can with regard to
Johne's disease.[312] The USDA,
for example, cites the formation of the National Johne's Working
Group in 1994. However, the executive committee of the group is
composed of three people: one is John Adams of the National Milk
Producers Federation and another is Gary Weber a director of the
National Cattleman's Beef Association.[313]

For those that remember the Oprah Winfrey mad cow fiasco,
Weber was the cattleman defending cow cannibalism. "Now keep in
mind," he said on that show, "before you--you view the ruminant
animal, the cow, as simply a vegetarian---remember that they drink
milk." Years earlier he told industry publication Food Chemical News
that the cattle industry could indeed find economically feasible
alternatives to feeding rendered animal protein to animals raised for
slaughter, but that the Cattlemen's Association did not want to "set
a precedent of being ruled by activists."[314]

Not surprisingly the National Johne's Working Group has
officially come out against making Johne's a reportable disease,
advocating that all attempts at control be voluntary.[315] In a moment of rare candor, one Working Group
member explained why: "If the farmers have to report positive cows,
then it will be like the sheep scrapie [mad sheep disease] program.
Instead of reporting the disease, the farmers will 'shoot, shovel and
shut up.'"[316]

A year earlier, a national paratuberculosis certification
program had been started in order to identify low risk herds, but
only 1% of dairy operations reported participating in the program,
citing associated costs.[317] Less
than 15% of the dairy producers appear to test for Johne's.[318] In 1997 the Johne's Working
Group set up a similar program designed to be more affordable,[319] but again chose to keep it
strictly optional, relying on the "livestock industry in each state
to sell its economic advantage to its members."[320] As a concession to the industry, there is
still no federally mandated Johne's Disease control program.[321] Some states have Johne's
control programs, but without exception they are noncompulsory.[322] Just as government deregulation
of industry may have led to the mad cow disaster in Europe, the lack
of industry accountability may also play a pivotal role in the human
consequences of the paratuberculosis epidemic.[323]

The United States is being left behind in the world-wide race
to eliminate paraTB.[324] The
Netherlands, one of Europe's largest dairy exporters, has pledged to
eradicate paratuberculosis by the end of this year by instigating a
compulsory eradication program.[325] "To minimize the risk of human exposure to
paratuberculosis" is one of the explicit reasons given for the Dutch
program.[326] Sweden seems to be
closest to winning the battle, probably because it was the first
country whose control efforts were non-voluntary.[327] Australia is currently also certifying herds
with a view to eradication.[328]
Although there are currently no restrictions on international trade
as a result of the disease,[329]
that may well change and potentially threaten America's $700 million
dairy product export industry.[330]

Mike Collins began his messages to both the Johne's Disease
Committee and the general session of the US Animal Health Association
with the same words "Don't shoot the messenger."[331] Rather than participating in serious dialogue
around the issue, the dairy industry has been accused of spending its
energies slinging mud at researchers in the field,[332] giving lip service and vainly hoping it just
all blows away.[333] Christine
Rossiter, senior extension veterinarian with the Cornell University
Veterinary Diagnostic Laboratory, told the Wisconsin
Agriculturist that those who decide to address the issue are put
at risk and there's "no value placed by the industry on a person who
wants to do something about Johne's. Nobody wants to take it on."[334]

At an international colloquium on paratuberculosis, Chiodini
expressed his view that the current focus of the American dairy
industry "could put the industry in the same light as the tobacco
industry, being accused of a cover-up and faced with all sorts of
liabilities."[335] Paul
Strandberg, Assistant Attorney General of the State of Minnesota
warned the Johne's Committee that if they chose to be less than
forthright about the possible link between milk and beef and Crohn's
Disease, they could wind up on "60 Minutes" in the middle of a media
circus.[336]

Off the Shelf USA

In order to put the problem in perspective and get the issue
out in the open, the consumer movement needs to get a study of retail
milk supplies in the US funded. That is the recommendation of the
Paratuberculosis Awareness and Research Association.[337] That is the recommendation of researchers in
the field.[338] Not only has
industry allegedly "totally ignored" this approach,[339] one observer wrote that it would be
"political suicide" for a researcher in the US to even suggest such a
thing.[340] However, there have
been two brave souls. Year after year, Chiodini and Hermon-Taylor,
world recognized authorities on MAP on Crohn's, have submitted
proposals to the USDA and to the FDA to test retail milk supplies,
and year after year their proposals have been rejected.[341]

At a meeting of the US Animal Health Association, a
resolution was debated on whether or not to recommend that the USDA
test retail dairy products in the United States for the presence of
live paraTB bacteria. John Adams, the National Milk Producers
Federation executive member of the Johne's Disease Working Group, was
quite vocal in his opposition: "The FDA has already stated their
position. They are confident that pasteurized milk is safe. We don't
need to test retail milk."[342]

Steve Merkel, a founding member of the Paratuberculosis
Awareness and Research Association and whose wife has suffered with
Crohn's disease since 1960,[343]
replied "With all due respect, sir, if milk is as safe as you say it
is, then retail testing will simply confirm that fact. Are you afraid
of retail milk testing because you are afraid of what you might
find?" The resolution was voted down by an overwhelming majority.[344]

The Paratuberculosis Awareness and Research Association kept
at it. Finally, in 1999, PARA successfully submitted two resolutions
to the Johne's Disease Committee, one recommending the testing of
retail milk and milk products for the presence of live MAP and
another recommending research to determine what cooking temperatures
are needed to reliably kill MAP in ground beef. Although both
resolutions passed unanimously in open committee, they were later
voted down behind closed doors. PARA saw this as the USAHA going on
record as deliberately choosing ignorance about the presence of MAP
in food products for human consumption.[345]

The United States Animal Health Association tried to justify
why the resolutions were quashed: "During the discussions of these
resolutions, there was much concern about the feasibility of
end-product testing of milk and meat for an organism that science has
not confirmed as being the cause of Crohn's in humans, and the usage
of this information." In the opinion of PARA, as expressed in a
letter to Animal Health Association President-elect, "this statement
presents USAHA as not only primarily self-serving, but further, is
blatantly contemptuous of both its own member producers and the
American public." The letter concludes "We at PARA are saddened that
USAHA has chosen to be part of the problem rather than part of the
solution."[346]

Gambling with Lives

The USAHA statement reveals the gamble the industry is
willing to take. In Britain, when asked what the industry planned to
do about paratuberculosis, spokespersons said that it was "something
that bears watching"[347] but that
they "preferred to defer action" until paraTB is proven to cause
disease in humans.[348] This
sounded all too familiar to the British public after the mad cow
debacle, where the beef industry made the same wager--and lost.[349] According to some social
science studies, it was the British public authorities' decade-long
insistence on the safety of beef that did the most damage to the
public trust.[350]

The American dairy industry is similarly gambling not only
with the health of consumers, but with their own financial health.
The financial impact of paraTB is enormous;[351] paratuberculosis currently costs the American
livestock industry over a billion dollars a year.[352] A collapse in consumer confidence could raise
that figure much higher.

"If MAP is ultimately shown not to be the cause of Crohn's
disease," Chiodini argues, "then the industries have taken the
appropriate position of 'lip-service,' to give an image of
concern."[353] If, however,--as
PARA phrased it in an open letter to the industry--"dairy products
become associated with the dreadful, life-destroying disease known as
Crohn's disease, your markets may also collapse and may never
recover. The image of dairy foods as being necessary for good
nutrition, carefully propagated and nurtured by you for decades, may
be destroyed."[354]

Other Dairy Products

It's not enough to test milk; we need to test other dairy
products as well. One third of cheese produced in the US is made from
raw unpasteurized milk, in which one could expect the highest levels
of paraTB bacteria.[355] Cheese
manufacturers rely on the salty acidic environment of cheese to
inhibit bacterial growth,[356] but
MAP is resistant to such conditions.[357] Even less robust mycobacteria can survive in
soft cheese for at least 3 months and in hard cheese for up to 10
months.[358] Reportedly, at the
University of Wisconsin, there is currently a research project which
is investigating the survival of Mycobacterium paratuberculosis in
cheese.[359]

Since MAP can survive freezing for at least a year,[360] products such as ice cream may
also be implicated.[361] Ice cream
may also come from less rigorously pasteurized milk.[362] Other dairy products like butter, yogurt, and
infant formula must also be high research priorities.[363]

Beef

The standard veterinary recommendation when a cow is
diagnosed with Johne's is to have her sent to slaughter. Beef from
Johne's cattle is not prevented from being sold for human consumption
because paratuberculosis is not officially considered a human
pathogen. End-stage animals, their bodies dripping with literally
trillions of paratuberculosis bacteria, are ground straight into
hamburger meat.[364] When Crohn's
patient advocates found out that infected tissue from animals with
severe clinical paratuberculosis were funneled into the human food
supply they were described as, not surprisingly, "abhorred and
nauseated."[365]

In the advanced stages of Johne's Disease, MAP bacteria
course through the cow's blood stream, infecting her internal organs,
and potentially her muscle tissue. Even if the muscle tissue didn't
contain large numbers of MAP before the infected cow's death, when
she's slaughtered it seems impossible to ensure that feces do not
contaminate the various tissues that are taken from her, as evidenced
by the numerous E. coli food poisoning deaths in recent years.[366] As a scientist put it:
"Consequently, both preharvest and postharvest contamination of food
products originating from cattle is plausible."[367]

Although Americans eat 2.6 billion pounds of culled dairy
cows annually, most hamburger meat comes from cattle raised for beef.
In 1984, about one percent of US beef cattle were found positive for
Johne's Disease. Research is ongoing at the USDA to determine the
current prevalence of Johne's Disease in beef cattle, but since
Johne's is such a hidden disease, is not reportable, and is not the
subject of a mandatory control program, one might suspect that the
incidence has increased significantly as it has in the dairy cattle
population.[368] In spite of this
situation, lack of awareness among beef producers is even greater
than in dairy producers. The USDA Center for Animal Health Monitoring
reports that 69.8% of US beef producers "had not heard of it
[Johne's] before." And less then 10% of producers had any knowledge
beyond name recognition.[369]

MAP bacteria probably survive standard cooking temperatures.
Mycobacterium paratuberculosis is the most heat resistant
mycobacterium present in retail beef.[370] Even well cooked meat may contain live
paraTB. The USDA recommends that hamburgers be cooked to 71o Celsius
(160o F). An unpierced roast or steak need only reach an internal
temp of 63o C (145o F). Studies show prolonged exposure to at least
74o (165o F) may be necessary to eliminate the paratuberculosis
bug.[371] Mycobacterium
paratuberculosis is also resistant to nitrites and the smoking
process used in sausage production.[372] MAP may contaminate other meats as
well--paratuberculosis is suspected in pigs and chickens.[373]

Milk may be more dangerous to consume than meat, though, in
regards to paratuberculosis. MAP is thought to survive digestion when
carried in a vehicle like milk, because--as designed by nature--milk
buffers the stomach environment to a near-neutral pH. In meat
however, MAP's ability to survive digestion by stomach acid is less
certain.

Water

Municipal water supplies must also be assessed for risk
because surface waters contaminated by agricultural run-off feed the
domestic water supplies of many communities in the US.[374] One of the reasons why paraTB
has been called a "superbug" is because of its ability to survive in
the environment for prolonged periods.[375] Mycobacteria like paraTB have survived on
this planet for over a billion years which has allowed them to
adapt.[376] In the environment,
MAP has a thick waxy cell wall which protects it[377]--it can last for 9 months in mud,[378] and almost year in manure[379] and two years in water.
Standard domestic water treatment such as filtration and chlorination
are probably ineffective against paraTB.[380]

There have been a few disconcerting[381] reports of MAP bacteria cultured from
drinking water, both in Europe[382] and from the water supply of a major American
city.[383] Europe's Drinking Water
Inspectorate has commissioned a study into the distribution and fate
of MAP in drinking water treatment;[384] the same inquiry should be happening here.

2000

The development last year with the most serious ramifications
was published in the April 2000 issue of the American Journal of
Gastroenterology. Knowing that cows with Johne'sdisease shed
paratuberculosis into their breast milk, researchers wondered whether
paratuberculosis bacteria could be detected in the milk of human
mothers with Crohn's disease. Researchers also knew that there were
reports of mothers with other mycobacterial diseases like leprosy
shedding bacteria into their milk. So they examined two mothers with
Crohn's who had just given birth and found paratuberculosis bacteria
growing in both the mothers' breast milk, but not in the breast milk
from control mothers without Crohn's. While breast feeding has not
been found to be a risk factor for Crohn's and may actually have a
protective effect,[385] the
presence of MAP in the breast milk of mothers with Crohn's not only
adds support to the role of MAP in the pathogenesis of Crohn's
disease,[386] but shows how new
generations could be exposed to paraTB.[387]

Recommendations for Action

Despite the fact that M. paratuberculosis is now a known
human pathogen, it continues to be tolerated in our food supply.[388] After finding of MAP in their
retail milk supply, the Food Safety Authority of Ireland now requires
that cattle infected with Johne's be excluded from the food supply.
The flesh from an infected cow is no longer considered fit for human
consumption and her milk is simply dumped.[389] Karen Meyer of PARA commented, "The
government of Ireland is to be commended for exercising the
precautionary principle. Instead of trying to sweep the problem under
the rug, they acted swiftly to give human health priority over
special interests."[390]

The paratuberculosis problem in Ireland is minimal compared
to that of the United States. According to the Chief Executive of the
Food Safety Authority, of the 7.6 million cattle in Ireland, there
are only 12 reported cases of Johne's disease. Nineteen percent of
Irish retail milk samples grew out live paraTB and researchers only
found12 cases of Johne's disease in the entire country. Obviously, as
the Food Safety Authority concedes, this may be an underestimate, but
in the United States the paratuberculosis problem is exponentially
worse. The estimated prevalence in the US is some 20,000 times
greater than that of Ireland.[391]

If any country should be preventing contamination of the
human food supply it should be the United States, which has the
highest prevalence of Johne's disease in the world.[392] At their Fall 2000 meeting, however, the
National Johne's Working Group continued to propose only voluntary
measures to protect cattle health and no measures to protect human
health.[393] The removal of
clinically infected animals from the human food supply alone has been
modeled as having a highly significant impact.[394] This could evidently be accomplished with
relative ease, but as yet there has been little effort to do so.[395] When asked how long it would
take to clean up America's herds if suddenly no milk from
Johne's-positive cows could be sold, one Johne's Disease Committee
member said "About six months."[396]

The consumer movement also needs to fight to make Crohn's a
reportable illness.[397] The
official FDA stance that pasteurization eliminates MAP is no longer
tenable and must be continuously confronted with the British retail
milk studies which put an end to the pasteurization debate once and
for all. An extensive Freedom of Information Act search must be
initiated to unearth suppressed documents. For example, seven years
ago Canada's agriculture department produced a food safety risk
assessment paper concluding that the paraTB-Crohn's link was
something about which to be concerned. The document, however, was
stamped "Protected. Not for Distribution" and was as such buried.[398] These are the kinds of
documents the consumer movement needs to get a hold of.

In Dr. Hermon-Taylor's view, "There is overwhelming evidence
that we are sitting on a public health disaster of tragic
proportions."[399] Europe's
Scientific Committee on Animal Health and Animal Welfare, however,
concluded that the currently available evidence was insufficient to
confirm or disprove the theory.[400] This uncertainly should not impede the
government from taking concrete steps to prevent further potential
human catastrophe. If the British government had acknowledged the
precautionary principle, millions of lives may have been saved. A
headline in The Times sums up an inquiry into the mishandling
of the mad cow affair released last year in Britain: "Lack of Proof
Led to Disaster."[401]

The precautionary principal is the basis for most European
environmental law and is playing an increasingly important role in
health policies worldwide.[402]
Basically it states "If one has a reasonable suspicion that something
bad might be going to happen, one has an obligation to try to stop
it."[403] An ounce of prevention
is worth a pound of cure.

On a Personal Level

On a personal level, the Crohn's advocacy group Action
Research recommends that people who want to reduce their risk of
infection or reinfection--especially those with Crohn's disease, or
their close relatives (who might be genetically pre-disposed)--should
stop eating dairy products unless they are effectively boiled
first.[404] PARA recommends that
cheese should be heated to the temperature of boiling water, 100o C
(212o F), to reduce the threat. Thus, grilling cheese under direct
heat for a few minutes (so that it "bubbles"), or cooking it in
oven-baked meals, such as oven-baked lasagna, should effectively
sterilize the cheese. The same applies to other dairy products, such
as milk, yogurt or butter.[405]

The reason the industry doesn't pasteurize all milk at that
temperature to be safe, is because it could affect the taste of the
milk. As the Irish Food Safety Authority put it, "there is an upper
temperature beyond which unacceptable changes to the taste of milk
start to occur."[406] Steve Merkel
of PARA would have governments mandate raising the minimum
pasteurization temperature to levels that ensured safety regardless,
"even if it means that milk doesn't taste the same as it did. Human
health must take precedence over taste."[407]

Stricter pasteurization may not be the answer, though.
Although there is recent evidence that living MAP bacteria cause
Crohn's,[408] even dead MAP may be
able to trigger disease.[409] For
example, one of the reasons that the vaccine for Johne's is so seldom
used is because it is so dangerous to handle.[410] Even though the vaccine is made out of killed
MAP bacteria, the human immune system can react so violently just to
the presence of MAP proteins, that accidentally injected into humans
(or purposefully into other primates), the MAP vaccine causes a
chronic progressive inflammation which can last for years[411] or may even necessitate
amputation of the injection site.[412] Closely related bugs like leprosy can have
similar effects.[4133] So even if
MAP is pasteurized to death, drinking the remnants of the bacteria
may still cause a problem.

With this in mind, it may be more prudent to avoid dairy
altogether. Although ingesting relatively few organisms may be able
to cause infection, the human infective dose is not known.[414] It is also not known how
heavily the milk supply is contaminated in this country. The most
esteemed pediatrician of all time, Dr. Benjamin Spock, advised that
children be raised vegan, with zero exposure to dairy products for a
variety of reasons.[415]
Especially considering the risk of paratuberculosis in milk, this
would seem sensible advice, particularly for children and
adolescents.[416] There is a wide
variety of dairy product substitutes--soy and rice milks, cheeses,
ice cream, yogurt, etc.--making animal derived dairy products
unnecessary.

Conclusion

The epidemic of Johne's disease, like that of mad cow
disease, is an indictment of factory farming.[417] Intensive confinement systems in animal
agriculture have been accused of not only threatening the global
environment, but public health as well.[418] The unnatural concentration of animals raised
for slaughter, for example, has led to other human tragedies
including the single worst epidemic in recorded world history, the
1918 influenza pandemic.[419] In
that case, the unnatural density and proximity of pigs and ducks
raised for slaughter led to the deaths of upwards of 40 million
people.[420]

This potential crisis is also an indictment of an industry
that continues to risk public safety and a government that seems to
protect business interests over those of the consumer. As Karen Meyer
recently told the LA Times, "There comes a point in time where
consumer health takes precedence over commercial concerns."[421]

Every few hours, another child in this country is diagnosed
with Crohn's disease and may be condemned to a life of chronic
suffering.[422] The balance of
evidence strongly suggests a causative link between Mycobacterium
paratuberculosis and Crohn's disease.423 This public health issue has
been at the periphery of the dairy industry's agenda for years, a
nagging concern on the back burner.[424] The consumer movement needs to move it to the
front burner and needs to turn up the heat.

[35] Paratuberculosis Awareness &
Research Association. "MAP in food: The case for retail testing."
Presented to the Food Safety Committee of the United States Animal
Health Association in October 1998.
http://www.crohns.org/foodsafety/retail.htm.

[39] NAID. "Crohn's Disease - Is
There a Microbial Etiology? Recommendations for a Research Agenda."
Conference was held in the Natcher Conference Center on the NIH
campus in Bethesda, Maryland on December 14th, 1998.

[51] NAID. "Crohn's Disease - Is
There a Microbial Etiology? Recommendations for a Research Agenda."
Conference was held in the Natcher Conference Center on the NIH
campus in Bethesda, Maryland on December 14th, 1998.

[52] Chiodini RJ. "M
paratuberculosis in Foods and the Public Health Implications."
Proceedings of the Fifth International Colloquium on
Paratuberculosis Chiodini RK, Hines ME, and MT Collins (Eds.)
Madison, WI: International Association for Paratuberculosis,
1996:353-365.

[54] Hermon-Taylor J, et al.
"Mycobacterium paratuberculosis Cervical Lymphadenitis Followed Five
Years Later By Terminal Ileitis Similar to Crohn's Disease."
British Medical Journal February 7th 1998.

[105] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[106] Collins, MT and EJB
Manning. "Johne's Disease: The International Perspective." Department
of Pathobiological Sciences. University of Wisconsin School of
Veterinary Medicine Madison, Wisconsin.

[107] Sartor, RB. "M
paratuberculosis in Foods and the Public Health Implications."
Proceedings of the Fifth International Colloquium on
Paratuberculosis Chiodini RK, Hines ME, and MT Collins (Eds.)
Madison, WI: International Association for Paratuberculosis,
1996:366-373.

[108] Jones PH, et al. "Chronic
Gastrointestinal Diseases in Dairy Farmers in England and the Welsh
Borders: Is there an Association Between Crohn's Disease and Bovine
Paratuberculosis?" 9th Symposium for the International Society for
Veterinary Epidemiology and Economics, August 6-11 in
Breckenridge, Colorado, 2000.

[115] Hermon-Taylor J, et al.
"Mycobacterium paratuberculosis Cervical Lymphadenitis Followed Five
Years Later By Terminal Ileitis Similar to Crohn's Disease."
British Medical Journal February 7th 1998.

[116] Maugh II, TH. "Spreading
a New Idea on Disease: Mounting Evidence May Link Viruses And
Bacteria to Everything from Gallstones to Alzheimer's." LA
Times http://www.sonic.net/melissk/spreadin.html 1999.

[117] "Crohn's Disease May Be
Caused By Bacteria Similar to TB Microbe." Biotechnology
Newswatch July 5, 1999:5.

[119] Maugh II, TH. "Spreading
a New Idea on Disease: Mounting Evidence May Link Viruses And
Bacteria to Everything from Gallstones to Alzheimer's." LA
Times http://www.sonic.net/melissk/spreadin.html 1999.

[185] "Some cases of Crohn's
Disease appear to respond to antibiotic treatment: Evidence suggests
that a mycobacterium has a role in the illness; investigators have
tested clarithromycin alone and in combination with rifabutin."
Infectious Disease News July 1996.

[164] This may be particularly
important in that the subjects were also given probiotics (like
acidophilus) which may confound the results per (Suenaga K, et al.
"Serum Antibodies to Mycobacterium paratuberculosis in Patients with
Crohn's Disease." Digestive Diseases & Sciences 44(1999):1202-7.)

[177] Maugh II, TH. "Spreading
a New Idea on Disease: Mounting Evidence May Link Viruses And
Bacteria to Everything from Gallstones to Alzheimer's." LA
Times http://www.sonic.net/melissk/spreadin.html 1999.

[186] Smith, KL and JS Hogan.
"Milk Quality - A Worldwide Perspective." Annual Proceedings of
the National Mastitis Council St. Louis, Missouri, 1998.

[187] Assuming a billion
lymphocytes/ml as a reasonable defining concentration of pus,
regulations per (Heeschen, W.H. 1997. Codex regulations and food
safety. Bulletin of the International Dairy Federation No.319/1997,
pp 24.), a standard 20 drops/ml, and a "glass" as 500 cc., Grade A
milk may have more than seven drops of pus per glass.

[200] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[214] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[226] Paratuberculosis
Awareness & Research Association. "MAP in food: The case for retail
testing." Presented to the Food Safety Committee of the United States
Animal Health Association in October 1998.
http://www.crohns.org/foodsafety/retail.htm.

[269] Hansen D and C Rossiter
"Clinical description and epidemiology of Johne's Disease in cattle."
National Johne's Working Group, a subcommittee of the Johne's
Committee of the U. S. Animal Health Association.

[284] Highly esteemed Professor
of Animal Science Temple Grandin describes the practice in Oliver W.
Sacks' An Anthropologist on Mars (1996): "That's one sad, unhappy,
upset cow. She wants her baby, hunting for it. It's like grieving,
mourning--not much written about it. people don't like to allow them
thoughts or feelings."

[304] Per (USDA: APHIS.
"Johne's Disease on U.S. Dairy Operations." National Animal Health
Monitoring System. October, 1997) an underestimate of 3.4% all dairy
cows infected. Per (Dargatz D, et al. "What Do I Need to Know About
Johne's Disease in Beef Cattle?" USDA:APHIS:VS.
http://www.aphis.usda.gov/vs/ceah/cahmN309.899 August 1999) .4% of
all beef cattle infected. Per (Institute of Medicine. The Use of
Drugs in Food Animals. Washington DC: National Academy Press,
1999)10 million dairy cattle, 100 million beef cattle in the US.

[307] Wells SJ. "Herd-Level
Risk Factors for Infection with Mycobacterium paratuberculosis in US
Dairies and Association between Familiarity of the Herd Manager with
the Disease or Prior Diagnosis of the Disease in that Herd and Use of
Preventive Measures." Journal of the American Veterinary Medical
Association 216(2000):1450-7.

[325] United States Animal
Health Association. "Report of the USAHA Committee on Food Safety."
Monday, October 5, 1998 in Minneapolis, Minn.

[326] Paratuberculosis
Awareness and Research Association. "Experts from around the world
gather to discuss Paratuberculosis, Johne's Disease and Crohn's
Disease." February 19 1999. http://www.crohns.org/media/colloq.htm

[337] Paratuberculosis
Awareness & Research Association. "MAP in food: The case for retail
testing." Presented to the Food Safety Committee of the United States
Animal Health Association in October 1998.
http://www.crohns.org/foodsafety/retail.htm.

[362] Paratuberculosis
Awareness & Research Association. "MAP in food: The case for retail
testing." Presented to the Food Safety Committee of the United States
Animal Health Association in October 1998.
http://www.crohns.org/foodsafety/retail.htm.

[374] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[377] Paratuberculosis
Awareness & Research Association. "MAP in food: The case for retail
testing." Presented to the Food Safety Committee of the United States
Animal Health Association in October 1998.
http://www.crohns.org/foodsafety/retail.htm.

[380] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[381] Sartor, RB. "M
paratuberculosis in Foods and the Public Health Implications."
Proceedings of the Fifth International Colloquium on
Paratuberculosis Chiodini RK, Hines ME, and MT Collins (Eds.)
Madison, WI: International Association for Paratuberculosis,
1996:366-373.

[382] "UK scientists link
Crohn's to superbug in cow's milk." Canadian Business and Current
Affairs v.32(22) June 11, 1996:52.

[391] 21,500 to be more exact,
dividing the US prevalence per (USDA: APHIS. "Johne's Disease on U.S.
Dairy Operations." National Animal Health Monitoring System. October,
1997.) by the Irish prevalence per ("Statement in Relation to UK MAFF
Announcement." Food Safety Authority of Ireland Press Release. 11
August 1998.)

[392] Paratuberculosis
Awareness & Research Association. "MAP in the United Kingdom."
http://www.crohns.org/government/uk.htm, 1999.

[413] NAID. "Crohn's Disease -
Is There a Microbial Etiology? Recommendations for a Research
Agenda." Conference was held in the Natcher Conference Center on the
NIH campus in Bethesda, Maryland on December 14th, 1998.

[414] Thompson DE. "The Role of
Mycobacteria in Crohn's Disease." Journal of Medical
Microbiology 41(1994):74-94.